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Background The survival impact of neutropenia in chemotherapy for advanced NSCLC has been well discussed. We retrospectively analyzed the contribution of the severity of neutropenia to the survival of the patients who were treated with carboplatin and paclitaxel. Methods We retrospectively reviewed the medical records of all patients with NSCLC who were treated from January 1999 to December 2010 in Kansai Medical University Takii Hospital. Patients were included in this study if they had an advanced NSCLC (IIIb or IV) that was treated with front-line chemotherapy with carboplatin and paclitaxel. Results 402 patients of NSCLC were treated in our hospital during above period. One hundred and sixty-seven patients were met to the eligible criteria. The median age was 65 (31–79). Female and male were 42 and 125 respectively. Adenocarcinoma, squamous cell carcinoma, and large cell carcinoma were 118, 44 and 4, respectively. Grade 3/4, 1/2 and 0 neutropenia were observed in 55.7, 23.4 and 21.0%, respectively. The overall response rates of the groups of grade 3/4, 1/2 and 0 neutropenia were 40.7, 38.5 and 21.9%, respectively. The MST for the patients of grade 3/4, 1/2 and 0 neutropenia were 13.3, 10.0 and 9.7 months, respectively. On univariate analysis, OS was significantly longer in the patients of grade 3/4 neutropenia than their counterparts (P = 0.0122). In addition, multivariate analysis revealed that the grade 3/4 neutropenia was an independent favorable prognostic factor for OS (HR: 0.357, P = 0.0005). However, there was no significant difference between grade 1/2 and 0 neutropenia. Conclusion The previous report showed that there was no significant difference between grade 3/4 and 1/2 neutropenia from the view point of survival benefit. However, our results clearly showed that only grade 3/4 neutropenia, other than grade 1/2, have survival implications for front-line chemotherapy for advanced NSCLC.

Background Hodgkin Reed–Sternberg (H-RS) cell is the tumor cell of classical Hodgkin disease (cHD), and their characteristics are still unclear. KM-H2 was established as an H-RS cell line from pleural effusion of a patient with cHD. We investigated the implications of extracellular matrix (ECM) for adhesion and function of H-RS cell. Methods Adhesion assay was carried out with the in situ crystal violet staining method. Cell staining was carried out using monoclonal antibodies conjugated with fluoro-dye. Stained cells were analyzed by a FACScan. Results We seeded KM-H2 onto the gelatin-coated or non-coated dish. KM-H2 cultured on a non-coated dish grown as a floating cell and formed a cell cluster (referred to hereafter as fl-KM-H2). However, KM-H2 tightly adhered onto the surface of dish and achieved a cell spreading following cultivation on a gelatin-coated dish for 24 h (referred to hereafter as ad-KM-H2). When KM-H2 was cultured on a gelatin-coated well, the significant increase of the number of the adhesive cell was observed. Moreover, ad-KM-H2 abundantly expressed E-cadherin whereas fl-KM-H2 lacked the expression of E-cadherin. Because E-cadherin was widely accepted hallmark of mesenchymal-to-epithelial transition (MET), we concluded that gelatin could promote EMT in KM-H2. These MET of KM-H2 was also induced by type I collagen and fibronectin. However, type IV collagen and laminin failed to promote MET. In addition, we found that the P38 MAP kinase inhibitor (SB202190) could inhibit MET without loss of cell viability. On the contrary, the inhibitors of Erk or Akt could not inhibit MET of KM-H2. In addition, we revealed that Serine 910 of FAK was constitutively phosphorylated in KM-H2. Conclusion ECM components could induce MET in KM-H2. Further investigation might become a milestone to explore an alternative molecular target for antitumor therapy.